Promotional price valid on web orders only. Your contract pricing may differ. Interested in signing up for a dedicated account number?
Learn More

SLC30A4 Polyclonal Antibody, Invitrogen™

Rabbit Polyclonal Antibody

Supplier:  Thermo Scientific PA539552

Catalog No. PIPA539552


Description

Description

Zinc is the second most abundant trace metal in the human body. It is an essential element, serving both a structural role, as in the formation of zinc fingers in DNA-binding proteins, and a catalytic role in metalloenzymes, such as pancreatic carboxypeptidases (e.g., MIM 114852), alkaline phosphatases (e.g., MIM 171760), various dehydrogenases, and superoxide dismutases (e.g., MIM 147450). SLC30A4, or ZNT4, belongs to the ZNT family of zinc transporters. ZNTs are involved in transporting zinc out of the cytoplasm and have similar structures, consisting of 6 transmembrane domains and a histidine-rich cytoplasmic loop (Huang and Gitschier, 1997 [PubMed 9354792]).[supplied by OMIM, Mar 2008].
TRUSTED_SUSTAINABILITY
Specifications

Specifications

SLC30A4
Polyclonal
Unconjugated
SLC30A4
ZNT4
Rabbit
Antigen affinity chromatography
RUO
22785, 64469, 7782
-20°C
Liquid
Immunohistochemistry (Paraffin), Western Blot
1 mg/mL
Dulbecco′s PBS with 150mM NaCl, 50% glycerol and 0.02% sodium azide; pH 7.4
O14863, O35149, O55174
SLC30A4
A synthetic peptide derived from the internal region of human SLC30A4
100 μg
Primary
Human, Mouse, Rat
Antibody
IgG
Product Suggestions

Product Suggestions

Videos
SDS
Documents

Documents

Product Certifications
Promotions

Promotions

Product Content Correction

Your input is important to us. Please complete this form to provide feedback related to the content on this product.

Product Title

By clicking Submit, you acknowledge that you may be contacted by Fisher Scientific in regards to the feedback you have provided in this form. We will not share your information for any other purposes. All contact information provided shall also be maintained in accordance with our Privacy Policy.

Your feedback has been submitted: Thank you for helping us improve our website.